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Photocatalytic water splitting has recently attracted increasing interests for solar to chemical energy conversion. Nevertheless, the high-efficiency process for photocatalytic water splitting is driven by recombination of photogenerated electron-hole pairs and the resultant low H 2 productivity. Herein, we demonstrate that P-doping induced positive charge centers (Pδ+) and indium vacancies (V In) in ZnIn 2 S 4 (ZIS) nanosheets can significantly promote photosplitting pure water to simultaneously produce H 2 and H 2 O 2. Microstructural and spectroscopic analysis suggest that Pδ+ and V In can trap photogenerated electrons and holes, respectively, as a result of enhanced separation of electron-hole pairs. The optimal catalyst of P-CoNi/ZIS displays a stoichiometric H 2 and H 2 O 2 productivity of 1228.7 and 1105.5 μmol h−1 g−1, respectively, with an apparent quantum efficiency of 6.2% at 365 nm. Impressively, H 2 productivity of P-CoNi/ZIS has surpassed most reported catalysts for photocatalytic pure water splitting. This work provides a unique strategy to create efficient photocatalyst for pure water splitting. [Display omitted] • P-doping induces positive charge centers (Pδ+) and indium vacancy (V In) in ZnIn 2 S 4. • Pδ+ and V In can facilitate the separation of photogenerated electrons and holes. • Stoichiometric H 2 /H 2 O 2 production from photocatalytic pure water splitting is realized. [ABSTRACT FROM AUTHOR]

[Display omitted] The tumor suppressor protein p53 participates in the control of key biological functions such as cell death, metabolic homeostasis and immune function, which are closely related to various diseases such as tumors, metabolic disorders, infection and neurodegeneration. The p53 gene is also mutated in approximately 50% of human cancer cells. Mutant p53 proteins escape from the ubiquitination-dependent degradation, gain oncogenic function and promote the carcinogenesis, malignant progression, metastasis and chemoresistance. Therefore, the stability of both wild type and mutant p53 needs to be precisely regulated to maintain normal functions and targeting the p53 stability is one of the therapeutic strategies against cancer. Here, we focus on compound-induced degradation of p53 by both the ubiquitination-dependent proteasome and autophagy-lysosome degradation pathways. We also review other posttranslational modifications which control the stability of p53 and the biological functions involved in these processes. This review provides the current theoretical basis for the regulation of p53 abundance and its possible applications in different diseases. [ABSTRACT FROM AUTHOR]